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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:374.)
© 2003 American Heart Association, Inc.

Editorials

Is There a Need for Cholesteryl Ester Transfer Protein Inhibition?

Paolo Parini; Lawrence L. Rudel

From the Metabolism Unit (P.P.), Center for Metabolism and Endocrinology, Department of Medicine, Karolinska Institute at Huddinge University Hospital, Huddinge, Sweden, and Arteriosclerosis Research Program (L.L.R.), Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to Dr Lawrence L. Rudel, Wake Forest University School of Medicine, Department of Pathology (Comparative Medicine), Medical Center Blvd, Winston-Salem, NC 27157-1040. E-mail lrudel@wfubmc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

For the past twenty years, LDL cholesterol (LDL-C) has been the primary target of therapeutic approaches to prevent coronary heart disease (CHD). Reduction of plasma LDL-C has been successfully achieved by lifestyle changes, treatment by HMG CoA reductase inhibitors, the statins, and most recently, with cholesterol absorption inhibition via ezetimibe.¹ However, the identification of HDL cholesterol (HDL-C) as an independent risk factor for CHD, with the recognition that higher plasma HDL-C is associated with a decreased incidence of coronary events,² has prompted research for new therapeutic agents that raise HDL-C. The hope is that raising HDL-C will signal an increase in the movement of cholesterol from the periphery back to the liver (the so-called reverse cholesterol transport or RCT pathway) and protection from CHD will follow. In the February issue of Atherosclerosis Thrombosis and Vascular Biology, Barter and colleagues³ provide an interesting review focusing on the plasma cholesteryl ester transfer protein (CETP) as a novel target for raising HDL-C thereby reducing CHD. Their suggestion is that the time may be right for clinical trials to test this concept. Should we support this position?

See February, page 160

CETP is a hydrophobic plasma glycoprotein, mainly synthesized in the liver, possessing the unique ability to facilitate the transfer of cholesteryl ester (CE). HDLs are lipoprotein particles formed in the plasma compartment.⁴ Apolipoprotein (apo)A-I interacts on cell surfaces with the ABCA1 transporter and becomes lipidated with phospholipid and cholesterol. Subsequently, the enzyme LCAT interacts with these newly formed lipoproteins and catalyzes the . . . [Full Text of this Article]

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